Treatment with several Wnt/β-catenin signaling pathway regulators can change the cellular reprogramming efficiency; however, the dynamics and role of endogenous Wnt/β-catenin signaling in reprogramming remain largely unanswered. Here we identify the upregulation of WNT2 and subsequent β-catenin nuclear accumulation as key events in reprogramming. Transient nuclear accumulation of β-catenin occurs early in MEF reprogramming. Wnt2 is strongly expressed in the early stage of reprogramming. Wnt2 knockdown suppresses the nuclear accumulation of β-catenin and reduces the reprogramming efficiency. WNT2 overexpression promotes β-catenin nuclear accumulation and enhances the reprogramming efficiency. WNT2 contributes to the promotion of cell proliferation. Experiments with several drugs that control the Wnt pathway also indicate the importance of β-catenin nuclear accumulation in reprogramming. Our findings reveal the role of WNT2/β-catenin signaling in reprogramming.

用几种Wnt /β-catenin信号通路调节剂治疗可以改变细胞的重编程效率。然而，内源性Wnt /β-catenin信号转导的动力学和作用在很大程度上仍未得到解答。在这里，我们确定WNT2的上调和随后的β-catenin核积累是重编程中的关键事件。β-catenin的瞬时核积累发生在MEF重编程的早期。Wnt2在重新编程的早期强烈表达。Wnt2组合式抑制了β-catenin的核积累并降低了重编程效率。WNT2的过表达促进β-catenin的核积累并提高重编程效率。WNT2有助于促进细胞增殖。使用几种控制Wnt途径的药物进行的实验还表明，β-catenin核积累在重编程中很重要。我们的发现揭示了WNT2 /β-catenin信号传导在重编程中的作用。